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Advances in Immunology and Inflammation During and After Infectious Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: 20 August 2025 | Viewed by 4864

Special Issue Editor


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Guest Editor
Unit of Infectious Diseases, Department of Medicine and Surgery, “Kore” University of Enna, Enna, Italy
Interests: HIV; metabolomics; antimicrobial stewardship; cardiovascular disorders in HIV
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

In recent years, our knowledge regarding the role of inflammation and immune response during and after infectious diseases has improved. For instance, let us refer to sepsis definition and pathogenesis, or to the COVID-19 emergency. But inflammation and immune response during and after infectious diseases can also lead to serious consequences, such as cancers, metabolic disorders, and cardiovascular diseases.

With this Special Issue, we aim to provide new insights into immune response and inflammation, and especially persistent inflammation, in infectious diseases. Moreover, we aim to shed light on the immune response mechanisms which might help in developing new treatment strategies.

Original and review articles, including basic studies, are all welcome to be submitted to this Special Issue. Research topics may include, but are not limited to, the following:

  • Molecular and cellular mechanisms governing the immune response to microorganisms;
  • Molecular and cellular mechanisms involved in persisting symptoms after the resolution of infection (i.e., long COVID-19);
  • Therapeutic application of molecular and cellular patterns.

Dr. Manuela Ceccarelli
Guest Editor

Manuscript Submission Information

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Keywords

  • bacterial infections
  • fungi infections
  • HIV
  • COVID-19
  • immune response
  • inflammation

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Published Papers (3 papers)

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Research

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15 pages, 3061 KiB  
Article
Antiviral Effect of Melatonin on Caco-2 Cell Organoid Culture: Trick or Treat?
by Milda Šeškutė, Dominyka Žukaitė, Goda Laucaitytė, Rūta Inčiūraitė, Mantas Malinauskas and Lina Jankauskaitė
Int. J. Mol. Sci. 2024, 25(22), 11872; https://doi.org/10.3390/ijms252211872 - 5 Nov 2024
Cited by 1 | Viewed by 1434
Abstract
Melatonin is a hormone naturally produced by the body that has recently been found to have antiviral properties. However, its antiviral mechanisms are not entirely understood. Using Caco-2 cells, we developed a gastrointestinal organoid model to investigate the impact of melatonin on cellular [...] Read more.
Melatonin is a hormone naturally produced by the body that has recently been found to have antiviral properties. However, its antiviral mechanisms are not entirely understood. Using Caco-2 cells, we developed a gastrointestinal organoid model to investigate the impact of melatonin on cellular organoid culture response to Poly I:C-induced viral inflammation in the gastrointestinal tract. Melatonin was found to have different effect when applied as a pretreatment before the induction of viral inflammation or as a treatment after it. Melatonin pretreatment after Poly I:C stimulation did not protect organoids from size reduction but enhanced cell proliferation, especially when lower (1 and 10 µM) melatonin concentrations were used. On the other hand, treatment with melatonin after the induction of viral inflammation helped to maintain the size of the organoids while reducing cell proliferation. In pretreated cells, reduced IFNLR1 expression was found, while melatonin treatment increased IFNLR1 expression and reduced the production of viral cytokines, such as IFNλ1 and STAT1-3, but did not prevent from apoptosis. The findings of this study emphasize the importance of type III IFNs in antiviral defense in epithelial gastrointestinal cells and shed more light on the antiviral properties of melatonin as a potential therapeutic substance. Full article
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Review

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16 pages, 2428 KiB  
Review
Virus-Induced Pathogenic Antibodies: Lessons from Long COVID and Dengue Hemorrhage Fever
by Der-Shan Sun, Te-Sheng Lien and Hsin-Hou Chang
Int. J. Mol. Sci. 2025, 26(5), 1898; https://doi.org/10.3390/ijms26051898 - 22 Feb 2025
Viewed by 1173
Abstract
Virus-induced antibodies represent a dual-edged sword in the immune response to viral infections. While antibodies are critical for neutralizing pathogens, some can paradoxically exacerbate disease severity through mechanisms such as antibody-dependent enhancement (ADE), autoantibody, and prolonged inflammation. Long coronavirus disease (COVID) and dengue [...] Read more.
Virus-induced antibodies represent a dual-edged sword in the immune response to viral infections. While antibodies are critical for neutralizing pathogens, some can paradoxically exacerbate disease severity through mechanisms such as antibody-dependent enhancement (ADE), autoantibody, and prolonged inflammation. Long coronavirus disease (COVID) and dengue hemorrhagic fever (DHF) exemplify conditions where pathogenic antibodies play a pivotal role in disease progression. Long COVID is associated with persistent immune dysregulation and autoantibody production, leading to chronic symptoms and tissue damage. In DHF, pre-existing antibodies against dengue virus contribute to ADE, amplifying viral replication, immune activation, and vascular permeability. This review explores the mechanisms underlying these pathogenic antibody responses, highlighting the shared pathways of immune dysregulation and comparing the distinct features of both conditions. By examining these studies, we identify key lessons for therapeutic strategies, vaccine design, and future research aimed at mitigating the severe outcomes of viral infections. Full article
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24 pages, 4314 KiB  
Review
Is the Complement System Dysregulated in Preeclampsia Comorbid with HIV Infection?
by Sumeshree Govender, Mikyle David and Thajasvarie Naicker
Int. J. Mol. Sci. 2024, 25(11), 6232; https://doi.org/10.3390/ijms25116232 - 5 Jun 2024
Cited by 2 | Viewed by 1507
Abstract
South Africa is the epicentre of the global HIV pandemic, with 13.9% of its population infected. Preeclampsia (PE), a hypertensive disorder of pregnancy, is often comorbid with HIV infection, leading to multi-organ dysfunction and convulsions. The exact pathophysiology of preeclampsia is triggered by [...] Read more.
South Africa is the epicentre of the global HIV pandemic, with 13.9% of its population infected. Preeclampsia (PE), a hypertensive disorder of pregnancy, is often comorbid with HIV infection, leading to multi-organ dysfunction and convulsions. The exact pathophysiology of preeclampsia is triggered by an altered maternal immune response or defective development of maternal tolerance to the semi-allogenic foetus via the complement system. The complement system plays a vital role in the innate immune system, generating inflammation, mediating the clearance of microbes and injured tissue materials, and a mediator of adaptive immunity. Moreover, the complement system has a dual effect, of protecting the host against HIV infection and enhancing HIV infectivity. An upregulation of regulatory proteins has been implicated as an adaptive phenomenon in response to elevated complement-mediated cell lysis in HIV infection, further aggravated by preeclamptic complement activation. In light of the high prevalence of HIV infection and preeclampsia in South Africa, this review discusses the association of complement proteins and their role in the synergy of HIV infection and preeclampsia in South Africa. It aims to identify women at elevated risk, leading to early diagnosis and better management with targeted drug therapy, thereby improving the understanding of immunological dysregulation. Full article
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